Abstract
Isolated superfused field stimulated biopsy specimens of human peripheral arteries and veins, preincubated with3H‐(‐)‐noradrenaline (NA) to label the neural stores of NA, were used to study the potency of dopamine (DA) and of NA as triggers of α‐adrenoceptor mediated negative feedback control of sympathetic neurotransmitter secretion, evoked by stimulation with trains of 300 shocks at 1 Hz. In this preparation DA was found to be only slightly less potent than NA in depressing both the secretion of3H‐NA, and the contractile response, evoked by nerve stimulation. DA depressed the contraction evoked by exogenous NA as well, but to a very much smaller extent. On the other hand, DA was a very weak agonist on the α‐receptors of the smooth muscle; nearly 1 000 times higher concentrations of DA were required to mimick contractions evoked by exogenous NA. The results show that the neural α‐receptor function involved in control of NA secretion differs considerably from the α‐receptors ofe.g.smooth muscle, with respect to sensitivity to DA. It seems possible that the observed depressing effect of DA on NA secretion may be of pharmacological and clinical interest; it may at least in part explain the vasodilating effect of DA infusions in man.

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